Phenotypic characterization of these mutants indicated that the RAD epistasis group comprised genes involved in NER.Mutants in the RAD epistasis group were defective in genetic recombination and DSB repair; and these genes are therefore believed to be required for recombinational DNA repair.Many of the genes in the RAD epistasis group were required for spontaneous andor damageinduced mutagenesis, suggesting their participation in biochemical events associated with altered replication delity.Other genes not designated as RAD loci are those encoding proteins involved in the repair of lesions induced by mono and bifunctional psoralens. It is pharmacologically active and at supranutritional dietary levels can prevent the development of many cancers, thus demonstrating chemoprevention andor carcinostatic activities. Several organoselenium compounds have been shown to have promising cancer preventing activity and some of them are used in the synthesis of pharmacologically active drugs. Mammalian distribution and purication and properties of pig liver enzyme.Biochemistry. Toxicology. Biochemistry. Biochemistry. Carcinogenesis. Toxicology. Biochemistry. Carcinogenesis. Epidemiology. Possible role of the protein in cancer etiology.Focus on antioxidant therapy.Nutrition. Carcinogenesis. Cancer Epidemiol. Biomarkers Prev. DNA damage and mutations of different types clearly accumulate with age in mammalian tissues.Human progeroid syndromes resulting in what appears to be accelerated ageing have been linked to defects in DNA repair or processing, suggesting that elevated levels of DNA damage can accelerate physiological decline and the development of agerelated diseases not limited to cancer.Higher DNA damage may trigger cellular signalling pathways, such as apoptosis, that result in a faster depletion of stem cells, which in turn contributes to accelerated ageing.Genetic manipulations of DNA repair pathways in mice further strengthen this view and also indicate that disruption of specic pathways, such as nucleotide excision repair and nonhomologous end joining, is more strongly associated with premature ageing phenotypes.Delaying ageing in mice by decreasing levels of DNA damage, however, has not been achieved yet, perhaps due to the complexity inherent to DNA repair and DNA damage response pathways.Another open question is whether DNA repair optimization is involved in the evolution of species longevity, and we suggest that the way cells from different organisms respond to DNA damage may be crucial in species differences in ageing.Ageing can be dened as a progressive deterioration of physiological function, accompanied by an increase in vulnerability and mortality with age. A major motivation for ageing research is that age is the greatest risk factor for many diseases, including most types of cancer.The gradual greying of the worlds population makes research into the mechanisms of ageing a pertinent medical, social and economic problem.Despite its importance and considerable progress in this area in the last few decades, however, ageing is still a mysterious process, whose fundamental causes are still strongly debated.One of the reasons why the mechanisms of ageing are poorly understood is the difculty in discerning cause from effect and focusing on the underlying processes of ageing rather than its manifestations, longevity is often used as a readout.Nonetheless, longevity, which can be dened as how long an organism lives and can be quantied for experimental cohorts as average or maximum longevity, can be inuenced by many factors independent of ageing.